Recent work with actin networks cross-linked by filamin A (FLNa) has replicated in vitro the high stiffness properties of living cells by pre-stressing the network. The differential stiffness in vitro increases dramatically for large pre-stresses. The key feature of the FLNa dimer appears to be the hinge sequence between repeats 15 and 16 (hinge 1), such as FLNb and recombinant FLNa (h-) lacking hinge 1 do not exhibit this property. This research will investigate my hypothesis that the presence of hinge 1 allows the actin network to become aligned in the direction of the applied stress, before the network ruptures. The stiffness of the network is then governed primarily by the stiffness of the actin filaments, rather than the more compliant cross-link. The effort will (1) correlate the observed strains and differential stiffness with the change in the geometry of the network and predict the compliance of the deformed network, (2) image stress and unstressed networks to verify the predicted deformation, (3) measure and model networks of recombinant forms of FLNa without hinge 1, with hinge 1 between different repeat domains, and additional repeats between the actin binding site and/or between hinge 2. [unreadable] [unreadable]